Chronic neonatal exposure of rats to low level concentrations produces animals which exhibit an exaggerated sensitivity to the arrhythmogenic activity of norepinephrine. This cardiotoxic effect occurs in rats whose blood lead levels never exceed 50 micro grams/dl, a level commonly considered to indicate minimal toxicity in humans. Because the enhanced response to norepinephrine involves both the direct and indirect (vagal reflex) effects of the catecholamine on the heart, it is felt that both the adrenergic and cholinergic nervous systems are involved. During the first 10 days of life, the critical period for lead exposure, important events occur in the development of the adrenergic and cholinergic nerves of the rat. Studies are therefore proposed to examine development of adrenergic and cholinergic nerves in lead-exposed animals. To investigate adrenergic development, the uptake of norepinephrine and basal norepinephrine concentrations will be examined in control and lead-exposed rat pups during the nursing period, and adults after a lead-free period. Cholinergic nerve development will be studied by examining the characteristics of muscarinic receptors from rats of various ages. Activities of acetylcholinesterase and choline acetylase, enzymes which catalyze the breakdown and synthesis of acetylcholine, respectively, will also be examined. Other agents known to produce cardiac arrhythmias will also be tested to determine the specificity of the cardiotoxicity due to lead exposure. This study should provide additional information regarding subclinical lead toxicity, and possibly new insights into autonomic nerve development.